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Please use this identifier to cite or link to this item: http://ntour.ntou.edu.tw:8080/ir/handle/987654321/26988

Title: Aquatic birnavirus infection activates the transcription factor NF-κB via tyrosine kinase signalling leading to cell death
Authors: J-R Hong;B-J Guan;G M Her;O Evensen;N Santi;J-L Wu
Contributors: NTOU:Institute of Bioscience and Biotechnology
國立臺灣海洋大學:生物科技研究所
Keywords: apoptosis;infectious pancreatic necrosis virus;NF-κB;proteasome inhibitors PSI-I and II;tyrosine kinase inhibitor genistein
Date: 2008-06
Issue Date: 2011-10-21T02:22:11Z
Publisher: Journal of Fish Diseases
Abstract: Abstract:Our previous studies found that infectious pancreatic necrosis virus (IPNV) induces host apoptotic cell death, possibly through a newly synthesized protein trigger. Here, we examine whether IPNV infection can induce NF-κB activation through tyrosine kinase signalling of CHSE-214 cell death (host cell death). Using the electrophoretic mobility shift assay (EMSA) to detect transcription factor activation, we found that NF-κB is apparently activated 6–8 h post-IPNV infection. Using genistein (100 μg mL−1; a tyrosine kinase inhibitor) to determine whether NF-κB activation requires tyrosine kinase activation, we found genistein blocks NF-κB activation at 8 h post-infection (p.i), and either enhances cell viability up to 50% at 12 h p.i. or blocks DNA fragmentation at 24 h p.i. Furthermore, the proteasome inhibitors PSI-I and PSI-II (both at 40 μm) also effectively blocked the NF-κB activation as well as stimulating a 30% increase in cell viability (30% decrease in apoptosis) at 8 and 12 h p.i. Taken together our data suggest that IPNV may induce NF-κB activation through tyrosine kinase signalling, which may be associated with induction of apoptosis.
Relation: 31(6), pp.451–460
URI: http://ntour.ntou.edu.tw/handle/987654321/26988
Appears in Collections:[生命科學暨生物科技學系] 期刊論文

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